全球气候治理新进展——区域碳排放权分配研究综述

碳排放权作为稀缺的公共资源,其实质是一种新型发展权。科学合理分配有限的碳排放权对实现《巴黎协定》温控目标至关重要。从原则、方法、尺度与方案等维度对碳排放权分配的文献成果进行了系统梳理与归纳。研究表明,国内外学者大多基于公平性和效率性原则探索碳排放权分配;分配方法分为指标法、博弈论法、数据包络分析法和综合法等,各有利弊和适用条件;分配尺度大多涉及国际和区际两个层面,前者由于各国不同的利益诉求较难形成共识性方案,后者主要关注省际分配,更小尺度的研究相对较少。未来碳排放权分配研究趋向于多原则兼顾、多方法联用,涵盖国际、省际、市际及行业、企业等不同尺度。本研究可为制定科学合理的碳排放权分配方案提供理论依据,为我国更为积极有效地参与全球气候治理提供决策参考。     

典型温带雨养泥炭沼泽湿地地下部二氧化碳和甲烷浓度变化规律及其影响因素

为研究北方泥炭沼泽湿地二氧化碳(CO₂)和甲烷(CH₄)浓度随深度的变化规律及其影响因素,选取欧洲北部典型雨养泥炭地贝尔山湿地(BBM)和舒特兹山湿地(SBM)两个采样点,通过原位采集泥炭剖面温室气体、孔隙水以及土壤样品,结合傅里叶变换红外光谱(FTIR)技术、碳氮同位素技术,探讨泥炭土壤的分解程度及温室气体浓度变化的关系。研究结果表明:(1)BBM采样点地下部的CO₂浓度变化规律总体呈现随深度波动减少趋势,值多在3000μmol/L附近波动,最大值为4210.74μmol/L(120 cm),SBM采样点的CO₂浓度随深度先增后减,60 cm以上在1800μmol/L附近波动,60 cm以下在3000μmol/L附近波动,最大值为4191.94μmol/L(90 cm);BBM和SBM地下部CH₄浓度都随深度增大,并且在60cm以下浓度增加较快,BBM最大值为735.90μmol/L(260 cm),SBM最大值为543.51μmol/L(170 cm)。(2)BBM和SBM...     

植物原生质体在分子细胞生物学研究中的应用

植物原生质体是去除了细胞壁的裸露细胞,其具有细胞全能性,现广泛应用于植物分子细胞生物学的研究中,可以大大缩减实验周期,并有助于得到体内实验的实时检测数据。该文除了介绍植物原生质体的提取和纯化方法外,还对国内外利用各种植物的原生质体进行细胞瞬时转化、亚细胞定位、细胞融合和大分子复合物相互作用等试验进行了总结和讨论。植物原生质体还可用于基因表达模式的实时检测,并作为生物反应器的受体细胞进行代谢物的体外生产。此外,还对当前该技术所面临的瓶颈进行了分析,为植物原生质体在分子细胞生物学领域的应用提供帮助,为技术的优化和推广提供参考。     

Syntaxin-1通过激活突触递质传递加速早期突触的形成

Syntaxin-1是一种多结构域蛋白,通过与synaptobrevin-2和SNAP-25形成SNARE复合体调节囊泡融合.然而,syntaxin-1在突触形成过程中是否发挥作用,目前尚不清楚.本研究显示syntaxin-1的表达水平与突触形成过程高度相关.Syntaxin-1的R151A和I155A突变影响其在突触形成中的促进作用,而Habc结构域或跨膜结构域在突触形成中无显著作用.结果表明,syntaxin-1通过激活突触囊泡释放来加速突触的形成.     

牛背梁自然保护区食肉目和偶蹄目动物的区系特征与生态分布

牛背梁自然保护区(108°45′~109°04′E,33°47′~33°56′N)位于秦岭山脉东段,地跨秦岭南北坡。采用样线调查法和访问调查法,于2003年5月~2004年8月,对该保护区食肉动物及偶蹄动物的区系特征和生态分布进行了研究。该保护区共有18种食肉动物及偶蹄动物,其中属我国级、级重点保护动物的兽类分别有2种和7种。分析表明,保护区的有蹄类动物物种丰富,秦岭分布的有蹄类在该区域均有分布,但食肉动物种数仅占整个秦岭地区的45.5%。这些兽类中,属于东洋界的兽类有12种,占66.7%;属古北界的仅1种,占5.5%;其余5种为广布种,占27.8%。牛背梁保护区在动物地理区划上应属古北界和东洋界物种交汇的区域,且为东洋界逐渐向古北界过渡的区域。分析该区域食肉动物及偶蹄动物的生态分布发现,这些物种的垂直分布幅度有很大的差异。垂直分布幅度在海拔高差1300m以上、1000m左右、450~700m之间的物种各占1/3。结果还表明,区内这些兽类物种的丰富度随海拔的升高具有先升后降的垂直变化规律。不论是秦岭南坡还是北坡,分布在海拔1800~2200m区域的兽类物种最多,所占比例大于80%;而在海拔2600m以上区域,兽类种数降至最少,仅占50%左右。兽类丰富度的海拔梯度也体现于这些兽类在各植被类型中的分布上。中山针阔叶混交林中分布的兽类种数最多,而在中低山落叶阔叶林、亚高山针叶林及亚高山灌丛草甸中分布的兽类则较少。     

Cryo-EM structure of glycoprotein C from Crimean-Congo hemorrhagic fever virus

Crimean-Congo hemorrhagic fever virus (CCHFV) is a causative agent of serious hemorrhagic diseases in humans with high mortality rates. CCHFV glycoprotein Gc plays critical roles in mediating virus-host membrane fusion and has been studied extensively as an immunogen. However, the molecular mechanisms involved in membrane fusion and Gc-specific antibody-antigen interactions remain unresolved largely because structural information of this glycoprotein is missing. We designed a trimeric protein including most of the ectodomain region of Gc from the prototype CCHFV strain, IbAr10200, which enabled the cryo-electron microscopy structure to be solved at a resolution of 2.8 ?. The structure confirms that CCHFV Gc is a class II fusion protein. Unexpectedly, structural comparisons with other solved Gc trimers in the postfusion conformation revealed that CCHFV Gc adopted hybrid architectural features of the fusion loops from hantaviruses and domain III from phenuiviruses, suggesting a complex evolutionary pathway among these bunyaviruses. Antigenic sites on CCHFV Gc that protective neutralizing antibodies target were mapped onto the CCHFV Gc structure, providing valuable information that improved our understanding of potential neutralization mechanisms of various antibodies.     

漆酶及其应用

结合当今该领域的最新研究进展,综述了漆酶来源、结构、作用机制、介体系统及其在水相和非水相中的应用,以期为漆酶催化性能的进一步研究提供一定的借鉴和参考.     

鱼腥藻PCC7120藻蓝蛋白α亚基体内重组研究

为了研究藻蓝蛋白α亚基的生物合成途径,通过构建相容的3种重组质粒pETDuet-cpcA、pCOLADuet-cpcE-cpcF和pACYCDuet-ho1-pcyA,将裂合酶基因cpcE和cpcF、血红素氧化酶基因ho1、藻蓝胆素合成酶基因pcyA和脱辅基藻蓝蛋白α亚基基因cpcA共同转入大肠杆菌BL21(DE3)。通过色素蛋白锌电泳和光谱检测表明产生了生物活性的CpcA-PCB。成功实现了大肠杆菌内藻蓝蛋白α亚基84位半胱氨酸残基与PCB的连接。而在裂合酶基因cpcE和cpcF不转入大肠杆菌的情况下,大肠杆菌内只有0.2%的CpcA-PCB产生。以上研究为进一步在大肠杆菌内合成天然的藻蓝蛋白奠定了基础。     

Inhibition of mitochondrial complex I improves glucose metabolism independently of AMPK activation

Accumulating evidences showed metformin and berberine, well‐known glucose‐lowering agents, were able to inhibit mitochondrial electron transport chain at complex I. In this study, we aimed to explore the antihyperglycaemic effect of complex I inhibition. Rotenone, amobarbital and gene silence of NDUFA13 were used to inhibit complex I. Intraperitoneal glucose tolerance test and insulin tolerance test were performed in db/db mice. Lactate release and glucose consumption were measured to investigate glucose metabolism in HepG2 hepatocytes and C2C12 myotubes. Glucose output was measured in primary hepatocytes. Compound C and adenoviruses expressing dominant negative AMP‐activated protein kinase (AMPK) α1/2 were exploited to inactivate AMPK pathway. Cellular NAD⁺/NADH ratio was assayed to evaluate energy transforming and redox state. Rotenone ameliorated hyperglycaemia and insulin resistance in db/db mice. It induced glucose consumption and glycolysis and reduced hepatic glucose output. Rotenone also activated AMPK. Furthermore, it remained effective with AMPK inactivation. The enhanced glycolysis and repressed gluconeogenesis correlated with a reduction in cellular NAD⁺/NADH ratio, which resulted from complex I suppression. Amobarbital, another representative complex I inhibitor, stimulated glucose consumption and decreased hepatic glucose output in vitro, too. Similar changes were observed while expression of NDUFA13, a subunit of complex I, was knocked down with gene silencing. These findings reveal mitochondrial complex I emerges as a key drug target for diabetes treatment. Inhibition of complex I improves glucose homoeostasis via non‐AMPK pathway, which may relate to the suppression of the cellular NAD⁺/NADH ratio.